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. 2022 May 4;13(5):435. doi: 10.1038/s41419-022-04886-7

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — A Representative microphotographs of H&E and Masson stainings of mouse models of bleomycin-induced pulmonary fibrosis group and control saline group. B Representative microphotographs of immunohistochemistry staining of P16, P21 and P53 in bleomycin-induced pulmonary fibrosis mouse model and control group. C β-gal staining was performed to mark senescent cells in lung tissue in bleomycin-induced mouse model and control group. D Western blotting was performed to evaluate the expression of P16, P21, KLF4, TERT, αSMA and Collagen-I expression in bleomycin-induced pulmonary fibrosis mouse and control group. E, F qPCR were performed to test P16, P21 and TERT in bleomycin-induced pulmonary fibrosis mouse and control group. G Double-labeled immunofluorescent staining were performed to examine the expression of SP-C (green) and TERT (red) in AECs between bleomycin-induced pulmonary fibrosis and control saline group. H Relative telomere lengths in lung tissues were tested in bleomycin group and control group. *P < 0.05, **P < 0.01, ***P < 0.001 by t-test.